Oral Administration Of Malathion Research Articles

Potential of rosmarinic acid to ameliorate toxic effects of diethyl methoxy thio‑phosphoryl thio‑succinate on albino wistar rats' lung, mast cell infiltration inhibitory pathway.

Malathion (MA) is a widely used pesticide in agriculture. It can cause toxicity in different organs of the body. Rosmarinic acid (RO) is found in rosemary extract that can be absorbed through gastrointestinal tract mucosa with potent antioxidant, and anti‐inflammatory potential. The current study is designed to investigate the potential of RO to protect the lung after MA administration. Forty albino rats were allocated equally to four groups. C‐group received corn oil. RO‐group received RO orally. MA‐group received MA. MA‐RO‐group received RO in addition to MA. After three weeks the lungs were dissected for histopathological and biochemical investigations. MA‐group showed manifestations of severe inflammation with inflammatory cells infiltration in the lung. MA‐RO‐group showed limited inflammatory cell infiltration. C‐group and RO‐group appeared with weak anti‐survivin immunoreactivity. MA‐group showed strong positive immunoreactivity. The reactivity was weakly positive in MA‐RO‐group. MA‐group showed a significant decrease in SP‐D gene expression in comparison to the C‐group, in addition, MA‐RO‐group showed a significant increase in SP‐D expression. In conclusion, the current study approves that oral administration of MA causes lung injury as it has inflammatory effects, caused by oxidative stress and reports the potential of RO to protect lung tissue against toxic effects of MA through its anti‐inflammatory, antioxidant, and anti‐apoptotic potential.

Histopathological changes of sub chronic toxicity induced by oral administration of Malathion in Rock dove pigeons (Columba livia)

The objective of the present study was to investigate the histopathological changes of the sub chronic toxicity of Malathion as organphosphorus insecticide in Rock dove pigeons ( Columba livia) treated orally with 6mg/kg and 4mg/kg body weight. The histopathological changes of central and peripheral nervous systems , liver, kidney, skin of pigeon after three month of treatment were included, marked vacuolation of nerve fibers of spinal cord and sciatic nerve, periportal fibrosis and liver congestion ,degenerate renal cortical tubules ,associated with loss of epithelial lining and disorganization of epithelial lining , and cortical areas of inflammatory cells with congestion of blood vessels, and dermal fibrosis and inflammatory cells of the skin

Oxidative stress and cholinesterase inhibition in saliva and plasma of rats following subchronic exposure to malathion

The aim of this study was to examine whether malathion, a commonly used organophosphate (OP), might induce oxidative stress and cholinesterase (ChE) depression in saliva and plasma in rats following subchronic exposure mimicking human exposure. Malathion was administered orally at doses of 100, 500 and 1500 ppm for 4 weeks. Oxidative stress was determined by measuring the malondialdehyde concentration, the end product of lipid peroxidation, and assessing total antioxidant power. Four weeks oral administration of malathion at doses of 100 ppm, 500 ppm and 1500 ppm depressed plasma ChE activity to 45% ( P<0.01), 48% ( P<0.01) and 41% ( P<0.01) of control, respectively. Malathion at doses of 100 ppm, 500 ppm and 1500 ppm depressed saliva ChE activity to 73% ( P<0.01), 75% ( P<0.01) and 78% ( P<0.01) of control, respectively. Malathion at doses of 100 ppm, 500 ppm and 1500 ppm increased plasma antioxidant power by 33% ( P<0.01), 59% ( P<0.01) and 118% ( P<0.01) of control, respectively. Malathion did not change saliva antioxidant power. Malathion at doses of 100 ppm, 500 ppm and 1500 ppm increased plasma thiobarbituric acid reactive substances (TBARS) by 61% ( P<0.01), 69% ( P<0.01) and 63% ( P<0.01) of control, respectively. Malathion at doses of 500 ppm and 1500 ppm increased saliva TBARS by 19% ( P<0.01) and 22% ( P<0.01) of control, respectively. Malathion (100 ppm) did not change saliva TBARS level. We concluded that in OP subchronic exposure, depression of ChE is accompanied by induction of oxidative stress that might be beneficial in monitoring OP toxicity.

Contribution of inflammatory mast cell mediators to alterations in macrophage function after malathion administration

Recent studies using mast cell-deficient mice showed that the presence of mast cells was necessary for the increase in macrophage function observed after oral administration of malathion and reconstitution with bone marrow-derived mast cells restored the ability of malathion to increase macrophage function. In addition, the release of mast cell mediators (blocked by cromolyn) and histamine (action blocked by pyrilamine) was shown to be involved in the action of malathion on macrophage function. In the present study, the contribution of inflammatory mediators (i.e. arachidonic acid metabolites and tumor necrosis factor [TNF]) which may be generated by mast cells after oral administration of malathion, was examined. Controls in this study included the effect of the agent to be examined on: (1) resident peritoneal macrophages; and (2) macrophages elicited with pristane, an agent shown previously to stimulate macrophage function in the absence of mast cells. Intraperitoneal administration of indomethacin, an inhibitor of cycloxygenase, or neutralizing antibody to TNF 30 h before and 4 h after oral malathion blocked the ability of malathion to increase macrophage function, as measured by the generation of respiratory burst activity and the production of cathepsin D. On the other hand, administration of these agents to mice injected intraperitoneally with pristane did not affect the observed increase in cathepsin D production. Respiratory burst function after elicitation with pristane was slightly decreased (indomethacin) or not affected (antibody to TNF). The effect of intraperitoneal administration of nordihydroguaiaretic acid (NDGA), an inhibitor of both cycloxygenase and lipoxygenase, was also examined. Intraperitoneal administration of NDGA partially blocked the effects of oral administration of malathion on peritoneal macrophage function, but did not affect the function of resident or pristane-elicited peritoneal macrophages. These data suggest that inflammatory mediators (potentially released from mast cells upon stimulation) contribute to the elevation in macrophage function observed after oral malathion administration.

Acute malathion toxicosis and related enzymatic alterations in Bubalus bubalis: antidotal treatment with atropine, 2-PAM, and diazepam.

Oral administration of malathion (MTH) in sublethal (100 mg/kg) or minimal lethal (125 mg/kg) doses in buffalo calves produced toxicity with an onset within 15-20 min and peak effects including severe tremors and convulsions within 40-60 min. Various antidotal drugs were administered alone or in combination at the time of peak malathion toxicity (within 1 h) and were assessed for their ability to alleviate signs of cholinergic toxicity. Blood cholinesterase and aminotransferases activities were monitored at various times. A combination of atropine sulfate (0.5 mg/kg, 1/4 iv and 3/4 im) and pyridine 2-aldoxime methiodide (2-PAM, 20 mg/kg, iv) reversed the clinical evidence of malathion toxicity within 15 min. The combination of atropine sulfate and diazepam (0.75 mg/kg, iv) prevented death and cholinergic signs of toxicity except for weak muscular fasciculations, which persisted for 30-60 min. Atropine sulfate alone was less effective and also did not reverse malathion-induced biochemical changes. In contrast, administration of either 2-PAM (10-30 mg/kg, iv) or diazepam (0.5-1.0 mg/kg, iv) alone accentuated malathion toxicity. Thus, the combination of atropine sulfate and 2-PAM was the most effective antidotal treatment in acute malathion toxicity.